Category: drugs

Although it is current practice to prescribe vitamin D and calcium together, particularly in post menopausal women, a six year study shows that the added calcium has no value.

The women were all over the age of 65 and had osteopenia. This is the stage before osteoporosis. 1,994 women were randomised to take zolendronic acid or placebo. Bone mineral density was measured at the spin, total hip, femoral neck and total body three times at intervals.

The baseline BMD was unrelated to dietary calcium after controlling for age, height, weight, physical activity, alcohol intake, smoking and past HRT use when a cross section of women were studied.

Loss of BMD over the next six years was not related to the amount of dietary calcium ingested.

And while we are on the subject of bones, I’m pleased to say that another study has shown that high dose vitamin D supplementation does NOT increase kidney stone risk.

Over just over 3 years of taking 100,000 iu of vitamin D3 each month did not increase excess calcium in the blood or the onset of kidney stones in adults aged between 50 and 84 years.

This dose is equivalent to 3300 iu vit D3 a day, similar to what many of us in the know take.

158 people took part in the randomised trial. The number of people developing kidney stones was similar in each group and no one in the intervention group developed hypercalcaemia. The groups self reported stones. No ultrasound was done which the authors say could have been more accurate.

Obesity is a major risk factor for type two diabetes and a cluster of metabolic factors that lead to poor cardiovascular outcomes. The amount of fat stored in the liver tissue closely mirrors insulin resistance and metabolic health.

Non alcoholic fatty liver disease (NAFLD) is now the commonest form of liver disease in the western world and can lead progressively to non alcoholic steatohepatitis (NASH), cirrhosis and hepatocellular carcinoma.

NAFLD is present in two thirds of obese people and promotes type two diabetes. NASH is present in half of these. NAFLD is expected to become the most common cause of liver transplantation by 2020.

Pioglitazone and the newer drugs such as Liraglutide (Victoza) can be used, as well as various dietary therapies.

If a weight loss of 10% can be achieved, there is a significant improvement in the inflammatory process that results in cell death and fibrosis in NASH. But weight loss is difficult to achieve and maintain. Pioglitazone can improve NASH in two thirds of non- diabetic patients and by around half in those with diabetes or pre-diabetes. Vitamin E has also been shown to have some success in non diabetic patients.

Liraglutide and drugs of the same class affect insulin secretion in response to meals, beta cell proliferation, inhibition of glucagon secretion, delayed gastric emptying, and making you feel fuller with less to eat.

These effects result in worthwhile clinical outcomes in overweight or obese patients whether they have diabetes or not. Body weight is reduced by at least 5% in 30% of patients and by at least 10% in 30% of patients. Over three years this can result in complete remission of the diabetes or pre-diabetes in 30% of the patients. Cardiovascular outcomes are also improved.

Triglyceride accumulation in the liver cells is the mechanism that has been recently shown to cause insulin resistant adipose tissue. After 48 weeks of high dose Liraglutide (1.8 mg a day), resolution of NASH was seen on biopsy samples in 39% of the treated group compared to 9% in the placebo group.

The main side effects are nausea and diarrhea. There could possibly be more gallstone development but no increase in pancreatitis.

Once more, dear friends, I’m putting my body to good use—a drugs trial where I hope my small part contributes to better outcomes for other people with diabetes.

Last year, when I received one of my six-monthly invites to the retinal screening clinic, an invite popped out of the envelope. Did I wish to take part in a trial for a drug aimed at preventing the progression of diabetic retinopathy? Not ‘alf. I’m keen to hang onto my eyesight for the rest of my life, especially as I’m a voracious reader.

I do have diabetic retinopathy. The changes to my eyes happened years ago, I’m screened regularly and while the letters that follow my appointments tell me there is more evidence of minor changes so far I’ve not needed treatment. And long may that happy state continue.

Cholesterol reducing

The drug I’ve been taking is a fenofibrate. I say that as if I have any idea of what that means. I don’t, apart from it belonging to the fibrate class of medications and it also has cholesterol reducing properties. I’ve now taken it for seven weeks.

If you are not familiar with drugs trial protocol, if a person is judged suitable for a trial after tests, they take the drug for a run-in period. Further tests are done—blood pressure, height, weight and bloods—and then you are put in one of two groups. One takes the real drug, the other takes a placebo and that’s you for two years.

I’ve done the run-in and now I’m about to do the two years around with the other thousand or so people who have been recruited to take part. Exciting to think our participation might shape treatments for years to come, and here’s hoping the drug proves effective not just for me but for anyone else at risk of losing their eyesight.